What is it about?
Nonsmall cell lung cancer (NSCLC) is highly malignant with limited treatment options, platinum-based chemotherapy is a standard treatment for NSCLC with resistance commonly seen. NSCLC cells exploit enhanced antioxidant defense system to counteract excessive reactive oxygen species (ROS), which contributes largely to tumor progression and resistance to chemotherapy, yet the mechanisms are not fully understood. Recent studies have suggested the involvement of histones in tumor progression and cellular antioxidant response; however, whether a major histone variant H1.2 plays roles in the development of NSCLC? This paper demonstrats a tumor-driving role of H1.2 in NSCLC, and reveals an antioxidant feedforward cycle coordinated by H1.2 and NRF2 (a master regulator of antioxidative response) which promotes tumor progression and chemoresistance.
Featured Image
Photo by Robina Weermeijer on Unsplash
Why is it important?
This work uncovers a tumor-driving role of H1.2 in NSCLC and indicates an “H1.2-NRF2” antioxidant feedforward cycle that promotes tumor progression and chemoresistance. In general, our findings demonstrated a previously unknown role of linker histone H1.2 in NSCLC and brought a diffferent angle into the molecular crosstalk between the linker histones, antioxidant defense system, and poor response to chemotherapy in NSCLC.
Perspectives
It is fascinating to me to think how linker histones function under different conditions, such as during tumor development and drug resistance. I hope you find this article thought-provoking.
Kun Huang
Huazhong University of Science and Technology
Read the Original
This page is a summary of: An antioxidant feedforward cycle coordinated by linker histone variant H1.2 and NRF2 that drives nonsmall cell lung cancer progression, Proceedings of the National Academy of Sciences, September 2023, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2306288120.
You can read the full text:
Contributors
The following have contributed to this page
